Any adverse effects of replacement vitamin C will be discuseed here. Topics include kidney stones, gall stones, oxidation, etc.
We plan to move good discussions from the General Topics forum here for posterity.

We have isolated and determined the structure of a new glycation product of lysine and dehydroascorbic acid. This compound was extensively degraded by irradiation with UVA light in the presence of a water-soluble human lens extract. Our results suggest that measurements of the amounts of advanced glycation end products in the eye lens could underestimate the extent of glycation, because of subsequent structural alterations due to UVA light. The damage of lens proteins in vivo therefore could be a result from the combined action of glycation and UVA light.

Vitamin C exists in two major forms. The charged form, ascorbic acid (AA), is taken up into cells via sodium-dependent facilitated transport. The uncharged form, dehydroascorbate (DHA), enters cells via glucose transporters (GLUT) and is then converted back to AA within these cells. Cell types such as certain endothelial and epithelial cells as well as neurons that are particularly prone to damage during diabetes tend to be those that appear to be dependent on GLUT transport of DHA rather than sodium-dependent AA uptake. We hypothesize that diabeticneuropathies, nephropathies and retinopathies develop in part by exclusion of DHA uptake by GLUT transporters when blood glucose levels rise above normal. AA plays a central role in the antioxidant defense system. Exclusion of DHA from cells by hyperglycemia would deprive the cells of the central antioxidant, worsening the hyperglycemia-induced oxidative stress level. Moreover, AA participates in many cellular oxidation–reduction reactions including hydroxylation of polypeptide lysine and proline residues and dopamine that are required for collagen production and metabolism and storage of catecholamines in neurons. Increase in the oxidative stress level and metabolic perturbations can be expected in any tissue or cell type that relies exclusively or mainly on GLUT for co-transport of glucose and DHA including neurons, epithelial cells, and vascular tissues. On the other hand, since DHA represents a signiﬁcant proportion of total serum ascorbate, by increasing total plasma ascorbate concentrations during hyperglycemia, it should be possible to correct the increase in the oxidative stress level and metabolic perturbations, thereby sparing diabetic patients many of their complications.

Another one, which finds new degradation products altho it doesn't discuss the impact:

METHODS. Human lens epithelial cells (HLE-B3) and rat lenses were exposed to hyperglycemic or oxidative stress in vitro or in vivo and probed for accumulation of F-ASA, fluoro-dehydroascorbate (F-DHA), fluoro-2,3-diketogulonate (F-DKG), and their degradation products in protein-free extracts, by proton-decoupled 750-MHz 19F-nuclear magnetic resonance (NMR) spectroscopy.

RESULTS. F-ASA and F-DHA were taken up into HLE B-3 cells by an Na+-dependent transporter. Their uptake was unexpectedly only slightly affected by hyperglycemia in vitro, unless glutathione was severely depleted. Glycemic stress catalyzed oxidation of F-ASA into a single novel F-compound at −212.4 ppm, whereas F-DHA and F-DKG were the major degradation products observed after GSH depletion. In contrast, F-ASA uptake was markedly suppressed in diabetic cataractous rat lenses, which accumulated both the F-DHA and the −212.4-ppm compound. In an unexpected finding, the latter formed only from F-ASA and not F-DHA or F-DKG, suggesting a novel pathway of in vivo F-ASA degradation. Both the cells and the intact rat and human lenses were permeable to several advanced F-ASA and F-DHA degradation products, except F-DKG. The unknown compound at −212.4 ppm was the only F-ASA degradation product that spontaneously formed in rabbit aqueous humor upon incubation with F-ASA.

CONCLUSIONS. These studies suggest the existence of a novel ascorbic-acid–degradation pathway in the lens and aqueous humor that is influenced by the nature of the oxidant stress. Under similar culture conditions, intact lenses are more prone to hyperglycemia-mediated oxidant stress than are lens epithelial cells, but both are permeable to various F-ASA degradation products, the structure and biological roles of which remain to be established.

This one says it occurs in anaerobic conditions:

From the book The Maillard reaction in foods and medicine

Dicarbonyl compounds, such as dehydroascorbate (DHA), 3-deoxyglucosone(3DG)'7 and methylglyoxal (MGO),11 are present in tissues at micromolar concentrations,are increased in blood of diabetic patients, and brown proteins efficiently under anaerobic conditions.

This one supports the idea that DHAA prevents nonenzimatic glycation:Inhibitory effects of pyridoxal phosphate, ascorbate and aminoguanidine on nonenzymatic glycosylation

Inhibitory effects of pyridoxal phosphate, ascorbate and aminoguanidine on nonenzymatic glycosylation @ 2002AbstractNonenzymatic glycosylation of serum albumin was studied in the presence of naturally occuring metabolites, pyridoxal, pyridoxal phosphate and ascorbate/dehydroascorbate, and a hydrazine compound, aminoguanidine. Pyridoxal, pyridoxal phosphate, ascorbate and dehydroascorbate, at concentrations of 0.1 mM or greater, significantly inhibited the nonenzymatic glycosylation of albumin. Aminoguanidine was the most potent inhibitor of nonenzymatic glycosylation and 54% or 85% inhibition occurred when 5 or 50 mM aminoguanidine, respectively, was present in the incubation mixture containing 20 mM glucose. A major effect of aminoguanidine was to lower the free glucose concentration in the incubation mixture by a direct reaction with glucose as judged by thin layer chromatography. The present studies suggests that vital metabolites such as pyridoxal phosphate and ascorbate may be potentially important in controlling glucose-induced nonenzymatic glycosylation of proteins. Pyridoxal phosphate forms a Schiff base with proteins as does glucose and therefore may be a preferable drug, over aminoguanidine which is a hydrazine, for inhibiting the effects of glucose-induced nonenzymatic glycosylation.

Another positive one:

INHIBITION OF PROTEIN GLYCATION AND ADVANCED GLYCATION END PRODUCTS BY ASCORBIC ACID AND OTHER VITAMINS AND NUTRIENTS @ 1996A number of vitamins and nutrients were found to be potent inhibitors of both the glycation reaction and the subsequent end products. The nutrients were effective at physiological concentrations and exhibited dose-response relationships. The inhibitors included ascorbic acid, tocopherol, pyridoxal, niacinamide, sodium selenite, selenium yeast, and carnosine. A significant correlation was found between the inhibition of glycation and the inhibition of AGE formation (p < 0.001). One of the nutrients, ascorbic acid, was used in a pilot study. Eighteen normal subjects, 7 college age and 10 middle age, were supplemented with 1000 mg of ascorbic acid in the form of Re-natured vitamin C for a period of 4 weeks. Serum protein glycation was decreased an average of 46.8% (p < 0.01). These results underline the importance of nutrition in diabetes and indicate the possibility of therapeutic use of these nutrients for the prevention of diabetic complications.

On the other hand, Chris Gupta has pagewhich discuss use of topical Vitamin C to fight glaucoma.

So, that radio talk seems to me like bias, altho it looks like results depend on the tissue type and that DHAA might cause some glycation in specific tissues in specific conditions (GSH and Oxygen starvation)

Very complex, but after I few reads I get the impression that the "(ascorbate induced) glycation" is a result of DHA, not AA, and/or depleted or absent glutathione.

Much of it involves lens samples from diabetic patients, who are demonstrably off kilter in their metabolism. It is likely safe to assume that none of the samples came from truly well nourished patients who were taking ascorbate at the levels most of us suppose to be "correct". In fact I ask "are there any such patients who have cataracts?" I read my first reports of low incidence of cataracts in people who consumed large quantities of ascorbate for long periods of time, ie>10years, c1975More of this includes lens samples from ascorbate producing critters, and most of those used are nocturnal, giving different results from diurnal animals.

This all very lab grade experimental, and while there are some apparent errors, typos, and procedures that seem suspect to me, Dr MO does in fact acknowledge most of this stuff, especially the questions. On balance, by my reading, the paper clearly shows that ascorbate is A GOOD THING, but maybe a problem when oxidised. The failure of oxidation correcting mechanisms for various reasons runs throughout the paper, as do implicit or explicit statements regarding various nutrients long believed to be important in cataracts and diabetes in particular. Notable are multiple B vitamins and trace metals. All in all, I think it interesting and valuable work looking for answers or at least clues.

A second paper is:http://www.iovs.org/content/41/6/1473.fullA study of ascorbate oxidation and metals, mainly copper. In this case, it appears that the oxidation is caused by copper and other things acting in the same way, in samples of cataracts. But, non cataractous lenses do not oxidise the ascorbate, so it seems that the ascorbate is being used up by the already sick lens.

This one is perhaps the current extreme of "Fun with Chemistry" . It uses a transgenic engineered mouse model with human, chick, synthetic, and rabbit bits to make a mouse that attained lens ascorbate and DHA levels 5-15 times human levels, in a creature that would normally have much lower levels, as it is nocturnal. These things are then cross/interbred with each other. The analysis involves more chemicals than God herself has to hand. The lenses are removed, beaten, homogenized, treated with all manner of stuff, frozen, etc., before being analyzed by similar means. One of the means used is NMR analysis tissue utilization of "ascorbate" modified by substitution of a fluorine or bromine atom into the structure - not the most inert of things to be meddling with.

Note that a number of the "evil" sequences cited in these papers involve lysine, so don't be surprised if we soon see attacks on that as well as ascorbate!

I admire the ingenuity, and desire to find information, of these people. I hope they know what it means, and most importantly, how or if to apply it someday. I do not think this is the day, and I find no indication that Dr MO does either.That leaves me with questions about the radio show, and Van's transcription; but, since I cannot listen to it, I'll just be puzzled as to how the academic papers seem to have turned into pop med advice.

Dr. Mark Obrenovich wrote:If someone is on chemotherapy and their chemotherapy mechanism of action is oxidative stress induced cytotoxicity then if you take too much vitamin C while having your chemo you could actually raise the therapeutic threshold of the dose... and require more of the chemotherapy to do its prospective effectiveness by taking too much vitamin C.

Is this interpretation of the data from Dr. Mark Obrenovich correct? Not according to Patrick Quillin inBeating Cancer with Nutrition (Patrick Quillin, 2005 edition, pp. 221-3).

Page 221:

Patrick Quillin wrote:Don't Take Your Vitamin C; Unless...

......A couple hundred thousand years ago, humans lost the ability to convert blood sugar (glucose) into vitamin C (ascorbic acid). Some scientists have called this evolutionary shift a figurative "fall from the Garden of Eden". All but a few creatures on earth produced their own vitamin C in massive quantities, with higher internal production when the creature gets sick. For instance, a 150 pound goat makes about 10,000 milligrams daily of vitamin C. Meanwhile, the Recommended Dietary Allowance for a 156 pound reference human is 60 milligrams per day.

......Vitamin C is one of the more utilitarian nutrients in the human body, by assisting in the construction of connective tissue (the glue that keeps the body together), regulating the levels of fats in the blood, assisting in iron absorption, aiding in the sythesis of various brain chemicals for thought, and protecting against the damaging effects of free radicals. In a study done at the University of California at Los Angeles, men who took supplements of 300 mg daily of vitamin C (5 times the RDA) live an average of 6 years longer than men who did not take supplements of vitamin C. Mark Levine, MD, researcher with the National Institutes of Health, finds evidence that 250 mg per day might be a more rational and healthy RDA for vitamin C.

Patrick Quillin wrote:......Meanwhile, oncologists worry about the possibility that vitamin C might inhibit the free radical activity of chemotherapy and radiation in destroying cancer cells. While it might seem logical that an antioxidant (like vitamin C) might reduce the effectiveness of a pro-oxidant (like chemo and radiation), the opposite has been found in animal and human studies: antioxidants protect the healthy tissue of the patient while allowing the cancer tissue to become more vulnerable to the damaging effects of chemo and radiation.

......In a study published in the Proceedings of the National Academy of Science, vitamin C always augmented tumor kill and never protected the cancer cells when scientists added various chemo and radiation therapies to cancer cells growing in a dish. In 2 major human cancer studies, adding vitamin C and other antioxidants to chemo and radiation improved patient survival, quality of life, and tumor kill.

......Then an unpublished research project from Sloan Kettering Cancer Hospital in New York found that cancer cells are "gluttons" for vitamin C, absorbing more than their fair share. The researchers concluded, though they never proved, that cancer patients should avoid vitamin C supplements while undergoing chemo and radiation. Dr. David Golde, author of the study even speculated: "The cancer cell wants vitamin C because it wants antioxidant protection." If cancer cells are looking for protection, then why is vitamin C the only antioxidant that they absorb? What about the 20,000 bioflavonoids (like quercetin), the 800 carotenoids (like beta carotene), vitamin E, lipoic acid, glutathione, and other antioxidants in the human body? Why do cancer cells only absorb vitamin C and not the others? The researchers admitted that vitamin C was being selectively absorbed by tumor cells because cancer cells are "sugar feeders" and think they are absorbing their preferred fuel, glucose (which is nearly identical in structure to vitamin C), when in fact they are absorbing vitamin C, an "Elvis impersonator" of sorts.

......Now let me weave all of this seemingly confusing data together to help make sense for the cancer patient. Any antioxidant can become a pro-oxidant in a given chemical soup. That is why Nature always gives us droves of different antioxidants to play "hot potato" with unpaired electrons until their destructive energy is dissipated. No food has just one antioxidant. No human cell wants just one antioxidant. Antioxidants can become pro-oxidants when in isolation, which is exactly what happens to cancer cells when they selectively absorb only vitamin C, hoping to get some fuel for growth. What really happens is the vitamin C quickly becomes a pro-oxidant, targeting its destruction exclusively for the cancer cells. Dozens of very well trained physicians have been giving high doses of intravenous vitamin C (10 to 100 grams daily) to thousands of cancer patients for decades with no side effects, and usually improved outcome. Intravenous vitamin C seems to have selective anti-cancer activity, according to an article in the Annals of Internal Medicine (Apr.6, 2004, p.533), authored by several doctors including researchers at the National Institutes of Health. Dr. Hugh Riordan has reported improved outcome in poor prognostic cancer patients who have been put in remission through use of high dose IV vitamin C.

Last edited by VanCanada on Fri Jan 13, 2012 11:48 am, edited 1 time in total.

Patrick Quillin wrote:......Vitamin C supplements can be helpful in slowing cancer, while making medical therapy more of a selective toxin against the cancer and protecting healthy host tissue. Vitamin C protects against heart disease, lengthens life span, and more...when taken in conjunction with a wide assortment of other antioxidants along with a good diet.

......A number of bright researchers have taken a tiny bit of knowledge out of context (vitamin C thickens artery walls, is selectively absorbed by tumors, can become pro-oxidant), then ASSUMED a sequence of unproven conclusions, without consulting the "prior art" in this field. Don't take your vitamin C supplements -- unless you want to live longer.

,,[Comment: I quoted the book as accurately as I could. However, the part above where he says "can become pro-oxidant" doesn't make sense to me in the context he's using it; but anyway I know what he's trying to say...Be well y'all.]

Physicians are advised to recommend that individuals increase their consumption of vitamin C rich foods as a means of reducing risk of H. pylori infection and as a possible means of mitigating the effects of infection in those with gastric disease who test positive tor H. priori. However, patients should be further advised to eliminate high-dose vitamin (intake while being treated with LAM triple therapy, to avoid any potential interference with the efficacy of the medication. It is known that low gastric pH is protective of H. pylori, which is why proton pump inhibitors to achieve neutral gastric pH are combined with antibiotics. From this preliminary research, prudent would suggest thai ascorbic acid (and perhaps other organic acids capable of lowering intragastric pH) should be avoided during and H. pylori therapy. Related research indicates that coadministration of probiotic flora to restore gut ecology can enhance clinical outcomes.---LAM ( lansoprazole , amoxycillin and metronidazole ) are reported above. However, research with amoxicillin, metronidazole, bismuth and omeprazole here (which was out after the book was written) concludes that Vitamin C is beneficial as addition to the treatment.

^^^More hogwash from the purveyors of drugs.^^^

"From: http://www.ncbi.nlm.nih.gov/pubmed/16708632"Performance of the proton pump and vitamin C metabolism in the stomach are closely mutually connected. Modification of hydrochloric acid secretion may affect gastric juice vitamin C concentration. Potentially disadvantageous influence of antisecretory drugs on the mechanisms of antioxidative protection in the stomach needs further investigation."

From: http://www.ncbi.nlm.nih.gov/pubmed/12827006"It is well known that chronic gastritis induced by Helicobacter pylori may be associated with hypochlorhydria and may also be accompanied by low levels of vitamin C in plasma and gastric juice in adults. This study investigates the relationship between H. pylori infection and vitamin C levels in the blood, plasma and gastric juice and the gastric juice pH of Korean children.""The data demonstrate that vitamin C levels in whole blood, plasma, and gastric juice and the gastric juice pH in Korean children are closely related to the severity of H. pylori infection and the histologic changes in the stomach. These data suggest that vitamin C may play a role in determining infection and progression, and vitamin C supplementation may be an important axis for the management of H. pylori infection in children."

From: http://www.ncbi.nlm.nih.gov/pubmed/9863475"Vitamin C may be protective against gastric cancer though infection with Helicobacter pylori is associated with a reduction in intragastric concentrations of vitamin C.""The reduction in gastric vitamin C concentrations is related to gastric juice pH, the severity and extent of gastritis, the presence of H pylori, and the CagA antibody status of the individual. These findings may have implications in H pylori associated carcinogenesis"

From: http://www.ncbi.nlm.nih.gov/pubmed/9926292"Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori (H. pylori) infection probably plays a role in gastric carcinogenesis. In vitro vitamin C has been shown to inhibit the growth of H. pylori. The aims of this study were to determine the effect of high dose vitamin C administration on H. pylori infection and on gastric juice total vitamin C concentration in patients with H. pylori related chronic gastritis. Sixty patients with dyspeptic symptoms and proven chronic gastritis and H. pylori infection, who were undergoing routine endoscopy, entered the study after giving informed consent. They were randomly coded into two treatment groups. Group 1 (controls, n = 28) were treated with antacids for 4 weeks and Group 2 (n = 32) received vitamin C 5g daily also for 4 weeks. Nine patients did not complete the study and were excluded. Plasma and gastric juice total vitamin C levels were measured at baseline, at the end of 4 weeks treatment and again 4 weeks after treatment cessation. In the control group H. pylori infection remained unchanged in all 24 patients throughout as did the mean gastric juice total vitamin C concentration. However, in the vitamin C treated group eight of 27 patients (30%) who completed the treatment course the H. pylori infection was eradicated (P = 0.01). In these patients the mean gastric juice total vitamin C concentration rose significantly from 7.2 +/- 1.6 micrograms/ml after 4 weeks treatment (P < M 0.001) and 19.8 micrograms/ml 4 weeks after treatment was discontinued (P < 0.001). In the remaining 19 patients with persistent H. pylori infection, the mean gastric juice total vitamin C concentration rose less than in those with successful H. pylori eradication; 6.3 +/- 1.7 micrograms/ml before treatment, 10.8 +/- 1.5 micrograms/ml after 4 weeks treatment (P < 0.05) and a return to pre-treatment levels (7.1 +/- 2.7 micrograms/ml) 4 weeks after vitamin C intake stopped. There were no side effects of vitamin C treatment. This study has shown that 4 weeks daily high dose vitamin C treatment in H. pylori infected patients with chronic gastritis resulted in apparent H. pylori eradication in 30% of those treated. In those patients there was also a highly significant rise in gastric juice total vitamin C concentration which persisted for at least 4 weeks after the treatment ceased. A significant, though less marked, gastric juice total vitamin C concentration increase was observed during vitamin C treatment even in subjects with persistent H. pylori infection, though this was not maintained after treatment ended. The mechanism whereby vitamin C treatment appeared to result in H. pylori eradication is unclear. "

In other words, treatment with 5gm/day can cure H Pylori, and "if you do not get the results you expect, you did not use enough or continue long enough." Dr F Klenner

From: http://www.ncbi.nlm.nih.gov/pubmed/11201681"Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori infection probably plays a role in gastric carcinogenesis. Vitamin C plays a role in the neutralization of various pathogenic factors connected with H. pylori infection, including the destruction of free radicals, which damage tissues and cell DNA, and inhibition of the formation of N-nitroso compounds, which have a strong carcinogenic activity. The aim of the study was to determine whether tobacco smoking had any effect on gastric juice vitamin C concentration in healthy subjects and in patients infected with H. pylori"

" These results demonstrate that the concentration of vitamin C in gastric juice is significantly lower in smokers than in non-smokers. This was observed in healthy subjects as well as H. pylori-infected patients. This phenomenon may be one of the mechanisms whereby smoking contributes to the production of gastric lesions, impairs healing of peptic ulcers and also increases the recurrence rate of peptic ulcers in cases with H. pylori infection."

So, they showed that smoking reduces vitamin C levels, which was known and quantified more than 60 years ago.They showed even better that H pylori is associated with very low vitamin C levels, but this is NOT pointed out.Of course, all this suggests that H pylori might be treated with vitamin C, as might some negative effects of smoking. That would of course require a total rethink of "their" views about vitamin C, would scuttle the drug treatment $$ of H Pylori, and shoot hell out of the anti tobacco industry.

gofanu wrote:Of course, all this suggests that H pylori might be treated with vitamin C, as might some negative effects of smoking. That would of course require a total rethink of "their" views about vitamin C, would scuttle the drug treatment $$ of H Pylori, and shoot hell out of the anti tobacco industry.

Administration of vitamin C, in a 5 g/day dosage during 28 days is neither effective for H. pylori eradication nor quantitatively alters the bacteria load in the stomach of infected patient

As far as I know acidic gastric environment is detrimental to h pylori and it tends to rise it up in order to survive which is why people get ulcers sometimes when they eradicate it (and probably have low levels of C, further attenuated by antibiotics). Also:

H. pylori synthesizes large amount of urease, which is found in its cytosol. The cytosolic urease is released into the gastric juice upon spontaneous autolysis of a subpopulation of H. pylori and subsequently it is adsorbed onto the surface of intact bacteria. The urease catalyses the hydrolysis of urea present in the gastric juice, to yield carbonic acid and ammonia. Thus H. pylori makes a cloud of ammonia on its surface to neutralize the gastric acid which enables it to colonize the gastric epithelium.[15,16] Once successfully colonized, H. pylori resides below the gastric mucus layer which has a higher pH than gastric lumen.[17,18] So in chronic infection, the role played by urease, in survival of the bacteria seems less important. However, besides protecting from acid, urease also aids in colonization by providing ammonia for bacterial protein synthesis

As far as I know acidic gastric environment is detrimental to h pylori

Medical dogma (prior to the Australian scientists Warren/Marshall?) was that bacteria could not survive in the acidic stomach environment. Most doctors trained prior to 1994 were taught this, which is one reason why the Australian work was ignored for so long. That was the break through - the reality that H Pylori can exist (thrive?) in stomach acid.

The medical establishment has made a complete mess of the vitamin c debate by referring to both AA and DHAA as vitamin c, again and again. What we have here with the medical establishment is a complete failure to communicate regarding DHAA, and the confusion has given vitamin c with an undeserved black eye, again and again. And I do think that the AA enthusiast community shares some blame by also referring to DHAA as "the oxidized form of vitamin c".

DHAA's pharmacokinetics is nothing like reduced vitamin c which comprises 99% of all vitamin c supplements. When you talk about DHAA you're talking about something most people can't even buy. That's why DHAA should never be referred to as vitamin c, not ever.

You don't refer to FeO2 as "iron", for heaven's sake, nor do you typically call it "oxidized iron" (that's a bar of iron with a thin layer of oxide), instead you refer to FeO2 as "iron-oxide" or "rust". Similarly we should insist that DHAA *never* be called "vitamin c" at any time, neither should it ever be called "oxidized vitamin c" (which can be a tablet of AA where the outside has turned yellow).

We should insist then on the medical community using the full name for DHAA, "dehydroascrobic acid", or "vitamin-c-oxide", or something entirely different preferably that sounds nothing like "vitamin c" (I have my own opinions what to call it, but they wouldn't be helpful).

In short, any drug contraindications with DHAA really shouldn't have any place in any discussion about vitamin c - I mean the typical consumer can't even buy the stuff. It's a paper tiger .. a straw man, used by the medical industry to discredit vitamin c. Don't take the bait - call it for the deception that it is and move on.

As for ulcers (presumably h.pylori ... but who knows) I can only provide my own testimony. I had blood in my bowels on and off for nearly a dozen years until I started megadosing c 10 years ago (at which time was getting progressively worse). Within days of megadosing the bleeding stopped. It returned one day 8 years later after I had stopped vitamin c supplementation for the first time in 8 years. I started megadosing that same day and in 24 hours it was gone and has not returned.

Bravo! You are so right, and I personally have never focused on this important distinction. (perhaps because unlike rust, DHAA can be reduced back to vitamin C, correct?) Anyway, if you want to turn this post into a short article, I would like to try to help get this published in the Townsend Letter as a letter to the editor. What do you think?

DHAA's pharmacokinetics is nothing like reduced vitamin c which comprises 99% of all vitamin c supplements. When you talk about DHAA you're talking about something most people can't even buy. That's why DHAA should never be referred to as vitamin c, not ever.

You don't refer to FeO2 as "iron", for heaven's sake, nor do you typically call it "oxidized iron" (that's a bar of iron with a thin layer of oxide), instead you refer to FeO2 as "iron-oxide" or "rust". Similarly we should insist that DHAA *never* be called "vitamin c" at any time, neither should it ever be called "oxidized vitamin c" (which can be a tablet of AA where the outside has turned yellow).

We should insist then on the medical community using the full name for DHAA, "dehydroascrobic acid", or "vitamin-c-oxide", or something entirely different preferably that sounds nothing like "vitamin c" (I have my own opinions what to call it, but they wouldn't be helpful).

ofonorow wrote:Bravo! You are so right, and I personally have never focused on this important distinction. (perhaps because unlike rust, DHAA can be reduced back to vitamin C, correct?) Anyway, if you want to turn this post into a short article, I would like to try to help get this published in the Townsend Letter as a letter to the editor. What do you think?

DHAA's pharmacokinetics is nothing like reduced vitamin c which comprises 99% of all vitamin c supplements. When you talk about DHAA you're talking about something most people can't even buy. That's why DHAA should never be referred to as vitamin c, not ever.

You don't refer to FeO2 as "iron", for heaven's sake, nor do you typically call it "oxidized iron" (that's a bar of iron with a thin layer of oxide), instead you refer to FeO2 as "iron-oxide" or "rust". Similarly we should insist that DHAA *never* be called "vitamin c" at any time, neither should it ever be called "oxidized vitamin c" (which can be a tablet of AA where the outside has turned yellow).

We should insist then on the medical community using the full name for DHAA, "dehydroascrobic acid", or "vitamin-c-oxide", or something entirely different preferably that sounds nothing like "vitamin c" (I have my own opinions what to call it, but they wouldn't be helpful).

Thanks Owen. I'd be happy to do that as it's something that I've festered over for some time. I'll PM you as I get close.